Β2 adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

Dayong Wang; Qin Fu; Yuan Zhou; Bing Xu; Qian Shi; Benedict Igwe; Lucas Matt; Johannes W. Hell; Elena V. Wisely; Salvatore Oddo; Yang K. Xiang

doi:10.1074/jbc.M112.415141

Β₂ adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

Dayong Wang, Qin Fu, Yuan Zhou, Bing Xu, Qian Shi, Benedict Igwe, Lucas Matt, Johannes W. Hell, Elena V. Wisely, Salvatore Oddo, Yang K. Xiang

Research output: Contribution to journal › Article › peer-review

79 Scopus citations

Abstract

Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β₂AR independently of presynaptic activities. Results: β₂AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β₂AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β₂ARs.

Original language	English (US)
Pages (from-to)	10298-10307
Number of pages	10
Journal	Journal of Biological Chemistry
Volume	288
Issue number	15
DOIs	https://doi.org/10.1074/jbc.M112.415141
State	Published - Apr 12 2013
Externally published	Yes

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

Access to Document

10.1074/jbc.M112.415141

Cite this

Wang, D., Fu, Q., Zhou, Y., Xu, B., Shi, Q., Igwe, B., Matt, L., Hell, J. W., Wisely, E. V., Oddo, S., & Xiang, Y. K. (2013). Β₂ adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models. Journal of Biological Chemistry, 288(15), 10298-10307. https://doi.org/10.1074/jbc.M112.415141

@article{63004817442048519eee40f8cdec6bc5,

title = "Β2 adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models",

abstract = "Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β2AR independently of presynaptic activities. Results: β2AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β2AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β2ARs.",

author = "Dayong Wang and Qin Fu and Yuan Zhou and Bing Xu and Qian Shi and Benedict Igwe and Lucas Matt and Hell, {Johannes W.} and Wisely, {Elena V.} and Salvatore Oddo and Xiang, {Yang K.}",

year = "2013",

month = apr,

day = "12",

doi = "10.1074/jbc.M112.415141",

language = "English (US)",

volume = "288",

pages = "10298--10307",

journal = "Journal of Biological Chemistry",

issn = "0021-9258",

publisher = "American Society for Biochemistry and Molecular Biology Inc.",

number = "15",

}

TY - JOUR

T1 - Β2 adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

AU - Wang, Dayong

AU - Fu, Qin

AU - Zhou, Yuan

AU - Xu, Bing

AU - Shi, Qian

AU - Igwe, Benedict

AU - Matt, Lucas

AU - Hell, Johannes W.

AU - Wisely, Elena V.

AU - Oddo, Salvatore

AU - Xiang, Yang K.

PY - 2013/4/12

Y1 - 2013/4/12

N2 - Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β2AR independently of presynaptic activities. Results: β2AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β2AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β2ARs.

AB - Background: Accumulating evidence indicates that βreceptors (βAR) may be involved in Alzheimer disease (AD) pathology and that amyloid βpeptide (Aβ) may interact with β2AR independently of presynaptic activities. Results: β2AR, PKA, and JNK mediate Aβ-induced phosphorylation of tau in vivo and in vitro. Conclusion: An Aβ-β2AR signaling is involved in tau pathology in AD. Significance: This work indicates a potential mechanism for altering AD pathology by blocking β2ARs.

UR - http://www.scopus.com/inward/record.url?scp=84876270805&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84876270805&partnerID=8YFLogxK

U2 - 10.1074/jbc.M112.415141

DO - 10.1074/jbc.M112.415141

M3 - Article

C2 - 23430246

AN - SCOPUS:84876270805

SN - 0021-9258

VL - 288

SP - 10298

EP - 10307

JO - Journal of Biological Chemistry

JF - Journal of Biological Chemistry

IS - 15

ER -

Β₂ adrenergic receptor, protein kinase a (PKA) and c-Jun N-terminal kinase (JNK) signaling pathways mediate tau pathology in alzheimer disease models

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this